interleukin-8 and Pleurisy

Thirty percent of patients with pneumonia develop pleural effusion, and of these, 20% have complicated effusion (CPPE), which may require a chest tube or surgery for resolution. The objective of the study is to compare the diagnostic yield of determining interleukin-1β and interleukin-8 in pleural fluid (PF) (PFIL-1β and PFIL-8) with respect to classic criteria (pH <7.2, lactate dehydrogenase [LD] >1,000 IU/mL, and/or glucose <60 mg/dL) in the early diagnosis of CPPE.. Of the 559 patients studied, 40 had CPPE. All underwent PF analysis: pH, glucose (PFGLUC), LD (PFLD), PFIL-1β and PFIL-8, and PF/serum ratios (PF/SIL-1β and PF/SIL-8).. The diagnostic criterion that showed the best area under the curve was the combination of PF/SIL-8 and PFIL-1β (0.906), with a statistically significant difference (P < .05) compared with the classic criterion of pH and PFGLUC or PFLD (0.826). The combination of PF/SIL-8 and PFIL-1β (cutoffs >5.73 and >9.14 pg/mL, respectively) was significantly more sensitive (72.7%) and more specific (97.9%) (P < .05) than the rest of the parameters used.. Measurement of IL-1β and IL-8 in pleural fluid may be useful in the early diagnosis of CPPE, although individually, it may not improve the results obtained with the PFLD. Further studies are needed to more firmly establish what role these new parameters can play in the diagnosis of CPPE.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Early Diagnosis; Empyema, Pleural; Glucose; Humans; Hydrogen-Ion Concentration; Interleukin-1beta; Interleukin-8; L-Lactate Dehydrogenase; Middle Aged; Pleural Effusion; Pleurisy; Pneumonia; ROC Curve; Sensitivity and Specificity; Young Adult

Several emerging lines of evidence support an anti-inflammatory role for nicotinamide and other vitamin B components. However, the mechanisms underlying their activity remain unclear. In the present study, we investigated the ability of nicotinamide to inhibit both neutrophil recruitment in IL-8-, LTB(4)- or carrageenan-induced pleurisy in mice and the rolling and adherence of neutrophils. Nicotinamide inhibited IL-8-, LTB(4)- and carrageenan-induced neutrophil migration, KC production and carrageenan-induced neutrophil rolling and adherence. We propose that the effects of nicotinamide in inhibiting neutrophil recruitment in carrageenan-induced pleurisy may be due to the ability of nicotinamide to inhibit the action of IL-8 and LTB(4), decrease KC production, and inhibit early events that regulate leukocyte migration from blood vessels into tissue.

Topics: Animals; Anti-Inflammatory Agents; Carrageenan; Cell Adhesion; Disease Models, Animal; Interleukin-8; Leukocyte Rolling; Leukotriene B4; Male; Mice; Mice, Inbred BALB C; Neutrophil Infiltration; Niacinamide; Pleurisy

The mechanisms of the systemic response associated with talc-induced pleurodesis are poorly understood. The aim of this study was to assess the acute inflammatory response and migration of talc of small size particles injected in the pleural space. Rabbits were injected intrapleurally with talc solution containing small or mixed particles and blood and pleural fluid samples were collected after 6, 24 or 48 h and assayed for leukocytes, neutrophils, lactate dehydrogenase, IL-8, VEGF, and TGF-beta. The lungs, spleen, liver and kidneys were assessed to study deposit of talc particles. Both types of talc produced an acute serum inflammatory response, more pronounced in the small particles group. Pleural fluid IL-8 and VEGF levels were higher in the small particle talc group. Correlation between pleural VEFG and TGF-beta levels was observed for both groups. Although talc particles were demonstrated in the organs of both groups, they were more pronounced in the small talc group. In conclusion, intrapleural injection of talc of small size particles produced a more pronounced acute systemic response and a greater deposition in organs than talc of mixed particles.

Topics: Acute-Phase Reaction; Animals; Biomarkers; Injections; Interleukin-8; Kidney; L-Lactate Dehydrogenase; Leukocyte Count; Leukocytes; Liver; Lung; Neutrophils; Particle Size; Pleural Effusion; Pleurisy; Pleurodesis; Rabbits; Spleen; Talc; Transforming Growth Factor beta; Vascular Endothelial Growth Factor A

Intrapleural talc is used to produce pleurodesis in malignant pleural effusions. Prior in vivo studies have documented an acute inflammatory response to talc in the pleural space but the cellular source of cytokines has not been identified. The aim of this study was to investigate the acute response of rabbit pleural mesothelial cells challenged with talc used for pleurodesis and compare it to prior studies of the response to talc in the rabbit pleural space. Cultured rabbit pleural mesothelial cells (PMC) were exposed to talc (25 mug/cm(2)) for 6, 24, or 48 h and assessed for viability, necrosis, and apoptosis by flow cytometry, Trypan Blue exclusion, and immunocytochemistry, and for the production of interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), and transforming growth factor-beta(1) (TGF-beta(1)) by ELISA. More than 50% of the PMC remained viable 48 h after talc stimulation. The PMC that were nonviable were identified as either apoptotic or necrotic, with roughly 20% in each category over the 48 h. At 6 h, the IL-8, VEGF, and TGF-beta(1) levels produced by talc-exposed PMC increased significantly and remained elevated for up to 48 h. These cytokine levels rose at similar times and at the same or higher levels than have been measured in the rabbit pleural space in prior studies. We report that viable, talc-exposed, pleural mesothelial cells may actively mediate the primary inflammatory pleural response in talc-induced pleurodesis.

Topics: Animals; Antiperspirants; Apoptosis; Cells, Cultured; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Epithelium; Immunohistochemistry; Interleukin-8; Pleura; Pleurisy; Pleurodesis; Rabbits; Talc; Transforming Growth Factor alpha; Vascular Endothelial Growth Factor A

Progelatinase B/proMMP-9 has recently been identified as an indicator of pleural inflammation, presumably originating from granulocytes. The aim of this study was to verify the origin of progelatinase B by simultaneous estimation of specific markers of neutrophil recruitment and activation in pleural effusions following induced pleurisy and pleural injury.. Sixty-three samples of pleural fluid from patients undergoing therapeutic talc pleurodesis (n = 8) and explorative thoracoscopy (n = 3) collected before and at different time intervals after the intervention were analyzed for progelatinase B and neutrophil gelatinase-associated lipocalin (NGAL)-gelatinase complex by substrate electrophoresis, for myeloperoxidase (MPO) and interleukin-8 (IL-8) by immunoadsorbent sandwich assay, as well as for leukocyte count, C-reactive protein (CRP) and total protein (TP).. A significant increase in free and NGAL-complexed progelatinase B, MPO and IL-8 was recorded within 48 h following treatment in all subjects. Progelatinase B was strongly correlated with NGAL-gelatinase complex (r = 0.88, p = 0.001), MPO (r = 0.81, p = 0.001), neutrophil count (r = 0.75, p = 0.01) and IL-8 (r = 0.71, p = 0.001), but not with CRP and TP.. The results support the neutrophil origin of the proenzyme, which confirms progelatinase B as an indicator of a local inflammatory reaction. Quantifying the inflammatory reaction may be helpful in the evaluation of both the technical variants of therapeutic pleurodesis and finer discrimination of paraneoplastic effusions.

Topics: Acute-Phase Proteins; Aged; Biomarkers; Cell Degranulation; Collagenases; Enzyme Precursors; Female; Gelatinases; Humans; Interleukin-8; Lipocalin-2; Lipocalins; Male; Matrix Metalloproteinase 9; Metalloendopeptidases; Middle Aged; Neutrophils; Peroxidase; Pleura; Pleural Effusion; Pleurisy; Proto-Oncogene Proteins

To explore the anti-inflammatory effect and possible mechanism of Xiaochaihu Decoction (XCHD) and the different herbal formulations of its components.. Rat model of pleuritis was established by thoracic injecting 0.2 ml of 1% carrageenan. Rats in the treated groups were medicated with XCHD (11 g/kg) and the different herbal formulations of its components respectively as follows: thorowax root-scutellaria root (A, 3.5 g/kg), fresh ginger-pinellia tuber (B, 3 g/kg), ginseng-licorice root-jujube (C, 4.5 g/kg), A + B (6.5 g/kg), A + C (8 g/kg) and B + C (7.5 g/kg), and those in the normal group and the model group were given equal volume of instilled water, by way of gastrogavage for successive 5 days. Modeling was performed 2 hrs after the last medication. The amount of pleurorrhea, and leucocyte (WBC), marrow peroxidase (MPO), tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in pleurorrhea, and serum level of interleukin-8 (IL-8) were measured 12 hrs after modeling.. As compared with the model group, all the parameters measured were lower in all the treated group (P < 0.05) , and IL-1beta content in pleurorrhea in the XCHD group and Group A, B and C were significantly lower (P < 0.01).. XCHD and the different herbal formulations have obvious anti-inflammatory effect, showing certain preventive and therapeutic effect on pleuritis. Among the different formulations, the XCHD, A, B and C had better effects. The effects might be related to inhibiting the increase of cytokines as TNF-alpha, IL-1beta, and IL-8 to suppress the activation, infiltration and wandering of leucocytes.

Topics: Animals; Anti-Inflammatory Agents; Carrageenan; Drugs, Chinese Herbal; Interleukin-1; Interleukin-8; Male; Pleurisy; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha

Heme, a ubiquitous iron-containing compound, is present in large amounts in many cells and is inherently dangerous, particularly when it escapes from intracellular sites. The release of heme from damaged cells and tissues is supposed to be higher in diseases such as malaria and hemolytic anemia or in trauma and hemorrhage. We investigated here the role of free ferriprotoporphyrin IX (hemin) as a proinflammatory molecule, with particular attention to its ability to activate neutrophil responses. Injecting hemin into the rat pleural cavity resulted in a dose-dependent migration of neutrophils, indicating that hemin is able to promote the recruitment of these cells in vivo. In vitro, hemin induced human neutrophil chemotaxis and cytoskeleton reorganization, as revealed by the increase of neutrophil actin polymerization. Exposure of human neutrophils to 3 microM hemin activated the expression of the chemokine interleukin-8, as demonstrated by quantitative reverse-transcription polymerase chain reaction, indicating a putative molecular mechanism by which hemin induces chemotaxis in vivo. Brief incubation of human neutrophils with micromolar concentrations of hemin (1-20 microM) triggered the oxidative burst, and the production of reactive oxygen species was directly proportional to the concentration of hemin added to the cells. Finally, we observed that human neutrophil protein kinase C was activated by hemin in vitro, with a K(1/2) of 5 microM. Taken together, these results suggest a role for hemin as a proinflammatory agent able to induce polymorphonuclear neutrophil activation in situations of clinical relevance, such as hemolysis or hemoglobinemia.

Topics: Actins; Animals; Chemotaxis, Leukocyte; Cytoskeleton; Enzyme Activation; Heme; Hemin; In Vitro Techniques; Inflammation; Interleukin-8; Male; Neutrophils; Pleurisy; Protein Kinase C; Rats; Rats, Wistar; Respiratory Burst; Reverse Transcriptase Polymerase Chain Reaction; Superoxides; Transcription, Genetic

An elevated level of adenosine deaminase (ADA) in pleural liquid has been considered as a supplemental diagnostic marker for tuberculous pleurisy. However, this is complicated by false-positives and -negatives. Recently, it has been revealed that various cytokines are intimately involved in the pathognomonic physiology of tuberculosis. In this study, interleukin-8 (IL-8), tumour necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma) were compared with ADA in pleural liquid of patients with inflammatory (21 cases), malignant (28 cases) and tuberculous (21 cases) disease. The pleural ADA, IL-8, TNFalpha and IFNgamma levels in the tuberculous group were higher than in the other three groups. Analysis of receiver operating characteristic (ROC) curves, to evaluate the utility of the various parameters, demonstrates values for the area under the curve (AUC) of 0.770, 0.875, 0.892 and 0.987, respectively for IL-8, TNFalpha, ADA and IFNgamma. No false-positives were encountered with IFNgamma and only one case with a small volume of pleural liquid was a false-negative. This indicates that IFNgamma is a very reliable marker of tuberculous pleurisy.

Topics: Adenosine Deaminase; Aged; Area Under Curve; Biomarkers; Female; Humans; Interferon-gamma; Interleukin-8; Male; Pleural Effusion; Pleural Effusion, Malignant; Pleurisy; Predictive Value of Tests; ROC Curve; Sensitivity and Specificity; Statistics, Nonparametric; Tuberculosis, Pleural; Tumor Necrosis Factor-alpha

Sclerosants such as tetracycline (TCN) have often been used in the control of malignant pleural effusions. Although the resultant inflammatory response is probably important in the ensuing pleural fibrosis, the signals responsible for the cellular influx into the pleural space following TCN instillation are not well understood. This study, therefore, sought to determine whether the chemokines interleukin-8 (IL-8), growth-related protein (Gro), and monocyte chemotactic protein-1 (MCP-1) were locally elaborated within the first 72 h following intrapleural TCN administration. TCN induced an exudative effusion with high lactate dehydrogenase activity. Although there was no significant change in the pleural fluid total leukocyte content, the median polymorphonuclear neutrophil concentration decreased from 1.067x10(6) to 2.03x10(5) cells x mL(-1) between 24 and 72 h, whereas the median macrophage concentration increased from 1.44x10(5) to 5.98x10(5) cells x mL(-1) over the same period. Furthermore, IL-8, Gro and MCP-1 concentrations decreased between 24 and 72 h. Immunocytochemistry indicated expression of IL-8 by pleural mesothelial cells 24 h, but not 72 h, following TCN administration. The data suggest that local elaboration of interleukin-8 and growth-related protein, in part of mesothelial origin, may influence neutrophil recruitment in tetracycline-induced pleuritis.

Topics: Analysis of Variance; Animals; Chemokine CCL2; Chemokines; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Female; Immunohistochemistry; Interleukin-8; Leukocyte Count; Neutrophils; Nuclear Proteins; Pleural Effusion; Pleurisy; Rabbits; Statistics, Nonparametric; Tetracycline

We investigated the involvement of IL-8 in the delayed vascular permeability (VP) in rabbit lipopolysaccharide (LPS)-pleurisy. Maximal level of interleukin-8 (IL-8) was detected in pleural fluid at 2 h after LPS injection and anti-IL-8 inhibited the delayed VP by 90%. Injection of homologous IL-8 induced VP, the time-course of which preceded that of LPS-induced delayed VP. Production of IL-8 in LPS-pleurisy was inhibited with anti-tumor necrosis factor alpha (TNF-alpha), whereas the production of TNF-alpha was not affected with anti-IL-8. Injection of IL-8 did not induce TNF-alpha production and anti-TNF-alpha had no effect on IL-8-induced VP. Injection of homologous TNF-alpha induced IL-8 production and VP, and TNF-alpha-induced delayed VP was blocked with anti-IL-8. These results indicate important roles of IL-8 in LPS-induced delayed VP and that TNF-alpha causes the delayed VP through the production of IL-8.

Topics: Animals; Capillary Permeability; Female; Interleukin-8; Lipopolysaccharides; Neutrophils; Pleurisy; Rabbits; Time Factors; Tumor Necrosis Factor-alpha

Increased levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) have been reported in various diseases, including lung cancer. The role of the soluble form of the IL-6 receptor (sIL-6R) remains to be explored. We therefore measured IL-6, IL-8 and sIL-6R in effusion fluid and blood serum of 10 lung cancer patients with carcinomatous pleurisy (5 men, 5 women, age 64.3 +/- 4.4 years) by enzyme-linked immunosorbent assays. Serum levels of healthy individuals served as control. Concentrations of sIL-6R were much higher in serum compared to pleural effusion fluids of tumor patients (25,698 +/- 1,993 vs. 9,438 +/- 1,407 pg/ml: p < 0.0001). In contrast, IL-6 and IL-8 were found at high concentrations in carcinomatous pleural effusions in comparison to serum (IL-6: 964 +/- 176 vs. 10.2 +/- 1.3 pg/ml, p < 0.0001; IL-8: 319 +/- 85 vs. 9.6 +/- 9.6 pg/ml, p < 0.0001). The serum concentrations of IL-6 were not significantly increased in lung cancer patients (10.2 +/- 1.3 pg/ml) in comparison to controls (7.3 +/- 1.0 pg/ml). IL-8 was detected in the serum of only 1 patient and in low levels in the serum of controls (8.0 +/- 1.5 pg/ml; all values are mean +/- SEM). We conclude from this study that decreased levels of sIL-6R, but increased levels of IL-6 and IL-8, are found in pleural effusion fluid of patients with lung cancer and carcinomatous pleurisy. The low sIL-6R levels in the presence of high IL-6 levels in pleural effusions and the high sIL-6R levels in the presence of low IL-6 levels in serum may suggest a downregulation of sIL-6R expression of sIL-6R shedding in the presence of excessive amounts of IL-6.

Topics: Aged; Down-Regulation; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interleukin-6; Interleukin-8; Lung Neoplasms; Male; Middle Aged; Pleural Effusion; Pleurisy; Receptors, Interleukin-6

Topics: Animals; Antibodies, Monoclonal; Bronchoalveolar Lavage Fluid; Capillary Permeability; Chemotaxis, Leukocyte; Disease Models, Animal; Endotoxins; Enzyme-Linked Immunosorbent Assay; Extravascular Lung Water; Humans; Interleukin-8; Leukocyte Count; Neutrophils; Pleurisy; Pneumonia, Aspiration; Rabbits

Gram-negative endotoxin induces production of the potent chemotactic factor interleukin-8 (IL-8) in vitro; however, the importance of IL-8 in endotoxin-induced inflammation in vivo is unknown. We asked whether IL-8 is an important contributor to chemotactic activity in acute inflammatory liquids formed in response to endotoxin, and, if present, what concentrations of IL-8 antigen are generated. For these studies, we cloned and expressed rabbit recombinant IL-8 (rrIL-8), developed specific anti-rabbit IL-8 monoclonal antibodies (mAb), and then used these reagents to develop assays to detect rabbit IL-8 bioactivity and measure rabbit IL-8 antigen. Escherichia coli endotoxin (20 ng/ml, n = 4, or 2,000 ng/ml, n = 4) was instilled into the pleural space of eight rabbits for 6 h. Rabbit IL-8 bioactivity in the endotoxin pleurisy samples was assayed by measuring the migration of rabbit neutrophils toward the pleural liquid under two different conditions: 1) after addition of an anti-IL-8 neutralizing mAb and 2) after desensitization of the neutrophils to rrIL-8. Addition of the anti-IL-8 mAb decreased neutrophil migration toward the pleural liquid by 65 +/- 13 and 75 +/- 22% (mean +/- SE, after 20 and 2,000 ng/ml endotoxin, respectively; P < 0.01 compared with a control mAb). Desensitization of neutrophils to rrIL-8 decreased their migration toward the pleural liquid by 72 +/- 5% (P = 0.03, compared with exposure of neutrophils to buffer alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Base Sequence; Blotting, Western; Body Fluids; Chemotactic Factors; Endotoxins; Interleukin-8; Male; Molecular Probes; Molecular Sequence Data; Pleura; Pleurisy; Rabbits; Recombinant Proteins

Although the potent neutrophil chemotaxin, IL-8, is a known product of endotoxin-stimulated cells in vitro, the contribution of IL-8 to neutrophil recruitment in Gram-negative endotoxin inflammation in vivo is unknown. To determine whether neutralization of IL-8 would decrease endotoxin-induced neutrophil influx, we generated neutralizing mAbs to rabbit rIL-8 for use in our rabbit model of endotoxin-induced pleurisy. One mAb, ARIL8.2, specifically inhibited both rabbit rIL-8-induced chemotactic activity and activation of the rabbit IL-8 receptor transfected in 293 cells. Anesthetized rabbits with in-dwelling pleural catheters received either neutralizing mAb (ARIL8.2; 1 mg/kg) or irrelevant isotype-matched mAb (anti-HIV gp120) i.v. 1 h before as well as intrapleurally (20 micrograms/ml) at the time of intrapleural instillation of Escherichia coli endotoxin (200 ng bilaterally). ARIL8.2 blocked 77% of endotoxin-induced neutrophil influx (21 +/- 2 (SE) x 10(6) (ARIL8.2) vs 91 +/- 15 x 10(6) (anti-gp120) (p < 0.0001)). By Western analysis, a band corresponding to rabbit IL-8 was detected in the pleural liquid of rabbits in both groups. By ELISA, however, the concentration of free, unbound IL-8 in the pleural liquid was significantly less in the ARIL8.2 group than in the anti-gp120 group for at least 4 h, confirming that ARIL8.2 bound the IL-8 generated in vivo during that time. We conclude that neutralization of IL-8 profoundly inhibits neutrophil recruitment in endotoxin-induced pleurisy indicating that IL-8 is a major chemotactic factor in this model of acute inflammation.

Topics: Animals; Antibodies, Monoclonal; Endotoxins; Enzyme-Linked Immunosorbent Assay; Interleukin-8; Male; Mice; Mice, Inbred BALB C; Neutrophils; Pleurisy; Rabbits; Recombinant Proteins; Species Specificity

Pleural effusions secondary to various diseases are associated with the presence of different inflammatory cells. The role of selective chemotactic cytokines in the recruitment of phagocytes to the pleural space is unclear. IL-8 and monocyte chemotactic peptide-1 (MCP-1) are recently described cytokines that are chemotactic for neutrophils and monocytes, respectively. We prospectively studied 63 patients, using strictly defined criteria for their selection. IL-8 concentrations were elevated in both empyema fluid (9.15 +/- 0.89 ng/ml) and parapneumonic effusions (4.7 +/- 0.697 ng/ml) when compared with pleural effusions secondary to other diseases. IL-8 levels were higher in empyema fluid than in parapneumonic effusions (p = 0.01). There was a significant correlation between IL-8 levels and the total numbers of neutrophils in empyema fluids (r = 0.80). Chemotactic activity for neutrophils was elevated in empyema fluid and the addition of IL-8 neutralizing serum decreased bioactivity by 32.22%. Malignant pleural effusions had the highest levels of MCP-1 (12.0 +/- 3.7 ng/ml) when compared with others. Cytology-positive pleural fluids (n = 10) had a higher level of MCP-1 than cytology-negative effusions (p = < 0.05). Malignant pleural fluid MCP-1 levels correlated (r = 0.70) with the absolute number of monocytes in the pleural fluid. Neutralization of monocyte chemotactic activity of malignant pleural fluid by specific neutralizing serum caused a 70.3% inhibition of bioactivity. Immunohistochemical staining of malignant pleural fluid localized antigenic MCP-1 to malignant cells. We conclude that both IL-8 and MCP-1 play major but not exclusive roles in the recruitment of neutrophils and monocytes from the vascular compartment to the pleural space.

Topics: Chemokine CCL2; Chemotactic Factors; Cytokines; Empyema; Heart Failure; Humans; Immunohistochemistry; Interleukin-8; Pleural Effusion; Pleural Effusion, Malignant; Pleurisy; Pneumonia; Tuberculosis, Pulmonary

Although acute asbestos-induced pleurisy is characterized by an influx of neutrophils, the identity of the factors that attract these cells to the pleural space and the source of the factors are unknown. We found that instillation of crocidolite asbestos into the pleural space of rabbits led to the appearance in pleural liquid of chemotactic activity for neutrophils, and that this chemotactic activity was inhibited significantly by a neutralizing antibody to human interleukin 8 (IL-8). Cultured rabbit pleural mesothelial cells incubated with crocidolite asbestos also released chemotactic activity for neutrophils, which was inhibited significantly by the anti-IL-8 antibody. To determine whether rabbit pleural mesothelial cells synthesize IL-8, we generated a probe for rabbit IL-8 mRNA by amplifying cDNA prepared from stimulated pleural mesothelial cells using the polymerase chain reaction (PCR) and primers based on homologous sequences in human and sheep IL-8 cDNAs. Homology-based PCR yielded a single cDNA fragment with a nucleotide sequence 88% identical to that of a corresponding region of human IL-8 cDNA. With the radiolabeled PCR product as a probe, we demonstrated rapid induction of IL-8 mRNA expression in pleural mesothelial cells exposed to asbestos. As expected, tumor necrosis factor-alpha also led to the appearance of IL-8 in the rabbit pleural space and stimulated cultured pleural mesothelial cells to synthesize and release IL-8. We conclude that asbestos directly stimulates pleural mesothelial cells to synthesize IL-8 and that mesothelial cell-derived IL-8 may play an important role in mediating asbestos-induced pleural inflammation.

Topics: Animals; Asbestos; Base Sequence; DNA; Epithelium; Interleukin-8; Male; Molecular Sequence Data; Pleurisy; Rabbits; RNA, Messenger; Tumor Necrosis Factor-alpha